Evidence map›Paper›PMID 21945077›Full record

ArticleDevelopmental biology2011

P190A RhoGAP is required for mammary gland development.

B M Heckman-Stoddard, T Vargo-Gogola, M P Herrick, A P Visbal, M T Lewis, J Settleman, J M Rosen

Abstract read
In one paragraph

Article in Developmental biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 29% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 34 citations in OpenAlex.

  1. Functions of RhoA in the female reproductive system.Reproductive and developmental medicine · 2025
    Review
  2. Article
  3. Article
  4. Article
  5. p190RhoGAPs, theCells · 2019
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. The RhoGEF Net1 is required for normal mammary gland development.Molecular endocrinology (Baltimore, Md.) · 2014
    Article
  11. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

B M Heckman-StoddardCancer Prevention Fellowship Program, Division of Cancer Prevention, National Cancer Institute, Bethesda, MD 20892, USA. heckmanbm@mail.nih.gov
T Vargo-Gogola
M P Herrick
A P Visbal
M T Lewis
J Settleman
J M Rosen
Baylor College of Medicine · USIndiana University School of MedicineNational Cancer Institute · US

Funding

TRANSFORMING GROWTH FACTOR ALPHA IN PATHOGENESIS OF BREAST CANCERP01CA030195 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI OESTERREICH, STEFFI · 1985 to 2009
$16.8M
Regulation of Mammary Stem CellsR01CA127857 · NCI · BAYLOR COLLEGE OF MEDICINE · PI LEWIS, MICHAEL T. · 2008 to 2012
$1.7M
P190-B RhoGAP regulates the microenvironment in the developing mammary glandR00CA127361 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI VARGO-GOGOLA, TRACY · 2009 to 2011
$740k
NCI NIH HHS CA030195-22NCI NIH HHS P01 CA030195NCI NIH HHS R00 CA127361NCI NIH HHS R00CA127361NCI NIH HHS R01 CA127857
6 · The paper itself

Abstract

P190A and p190B Rho GTPase activating proteins (GAPs) are essential genes that have distinct, but overlapping roles in the developing nervous system. Previous studies from our laboratory demonstrated that p190B is required for mammary gland morphogenesis, and we hypothesized that p190A might have a distinct role in the developing mammary gland. To test this hypothesis, we examined mammary gland development in p190A-deficient mice. P190A expression was detected by in situ hybridization in the developing E14.5day embryonic mammary bud and within the ducts, terminal end buds (TEBs), and surrounding stroma of the developing virgin mammary gland. In contrast to previous results with p190B, examination of p190A heterozygous mammary glands demonstrated that p190A deficiency disrupted TEB morphology, but did not significantly delay ductal outgrowth indicating haploinsufficiency for TEB development. To examine the effects of homozygous deletion of p190A, embryonic mammary buds were rescued by transplantation into the cleared fat pads of SCID/Beige mice. Complete loss of p190A function inhibited ductal outgrowth in comparison to wildtype transplants (51% vs. 94% fat pad filled). In addition, the transplantation take rate of p190A deficient whole gland transplants from E18.5 embryos was significantly reduced compared to wildtype transplants (31% vs. 90%, respectively). These results suggest that p190A function in both the epithelium and stroma is required for mammary gland development. Immunostaining for p63 demonstrated that the myoepithelial cell layer is disrupted in the p190A deficient glands, which may result from the defective cell adhesion between the cap and body cell layers detected in the TEBs. The number of estrogen- and progesterone receptor-positive cells, as well as the expression levels of these receptors was increased in p190A deficient outgrowths. These data suggest that p190A is required in both the epithelial and stromal compartments for ductal outgrowth and that it may play a role in mammary epithelial cell differentiation.

Indexed as

AnimalsBase SequenceDNA PrimersEpitheliumFemaleGene Expression Regulation, DevelopmentalGTPase-Activating ProteinsHeterozygoteHomozygoteIn Situ HybridizationMammary Glands, AnimalMiceMice, Inbred C57BLMice, KnockoutPregnancyReceptors, SteroidArhgap35 protein, mouseDNA PrimersGTPase-Activating ProteinsReceptors, SteroidRepressor Proteins

Identifiers

PMID21945077
PMCPMC3215776
OpenAlexW2029529001

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.